髓鞘少突胶质细胞糖蛋白抗体相关疾病磁共振特征分析
Analysis of magnetic resonance imaging characteristics in Chinese patients with myelin oligodendrocyte glycoprotein antibody associated disorders
摘要目的 探讨髓鞘少突胶质细胞糖蛋白抗体相关疾病(MOGAD)患者头颅和脊髓磁共振(MRI)病灶特征.方法 回顾性分析2013年9月至2017年12月就诊于中山大学附属第三医院神经内科的49例MOG-IgG阳性患者头颅和脊髓MRI结果,并与同期58例水通道蛋白4(AQP4-IgG)阳性患者进行比较分析.结果 两组患者头颅MRI检查出现异常病灶的比例差异无统计学意义(69.4%比65.5%,P=0.177),而AQP4-IgG组出现脊髓病灶的比例显著高于MOG-IgG组(84.5%比36.7%,P=0.001);MOG-IgG组出现皮质下白质病灶和大面积病灶的比例显著高于AQP4-IgG阳性组(48.9%比13.8%,P=0.003;46.9%比12.1%,P=0.000);AQP4-IgG组出现长节段横贯性脊髓病灶比例显著高于MOG-IgG组(70.7%比24.5%,P=0.002).儿童组患者中,MOG-IgG头颅出现大面积病灶的比例明显高于AQP4-IgG组(76.9%比20.0%,P=0.047).结论 MOGAD患者头及脊髓MRI病灶广泛,与AQP4-IgG阳性患者有差异.
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abstractsObjective To investigate the magnetic resonance imaging (MRI) characteristics in the brain and spinal cord of Chinese patients with myelin oligodendrocyte glycoprotein antibodies associated diseases (MOGAD).Methods Forty nine MOGAD patients with seropositive MOG-IgG and 58 AQP4-IgG positive patients were enrolled in this study.The characteristics of brain and spinal cord MRI were retrospectively analyzed.Results There was no significant difference in the proportion of abnormal brain MRI of the two groups (69.4% vs 65.5%,P=0.177),while the proportion of abnormal spinal cord MRI of the AQP4-IgG positive group was significantly higher than that in the MOG-IgG positive group(84.5% vs 36.7%,P=0.001).The proportion of MOG-IgG positive patients with subcortical white matter lesions and large lesions in the brain MRI was significantly higher than that in AQP4-IgG positive group(48.9% vs 13.8%,P=0.003,46.9% vs 12.1%,P=0.000).The longitudinally extensive transverse myelitis in spinal cord MRI of AQP4-IgG positive group was significantly higher than that in the MOG-IgG group(70.7% vs 24.5%,P=0.002).In addition,the proportion of MOG-IgG positive child patients with large lesions in the brain was significantly higher than that in AQP4-IgG positive child patients (76.9% vs 20.0%,P=0.047).Conclusion Demyelinating MRI lesions caused by MOG-IgG are heterogeneous,and could lead to a wide range of clinical phenotypes which is significantly different from those with AQP4-IgG.
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